everything about crps.

1. Complex Regional Pain Syndrome
(CRPS)
Dr Ravi shankar sharma
Daradia Pain Clinic
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3. Definition
The term complex regional pain syndrome (CRPS)
describes “a variety of painful conditions following
injury
 which appears regionally having a distal
predominance of abnormal findings,
 exceeding in both magnitude and duration of the
expected clinical course due the inciting event
 often resulting in significant impairment of motor
function, and showing variable progression over
time.”
-------- IASP

4. Epidemiology
• Females > males 2-4:1
• Preceding event: Fracture, surgery, minor
trauma
• No relation b/w severity of trauma and
presentation
• Across all ages, peak 50-70 yrs
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5. Types
These chronic pain syndromes comprise
different clinical features, including spontaneous
pain, allodynia, hyperalgesia, edema, autonomic
abnormalities, and trophic signs.
• CRPS type I (reflex sympathetic dystrophy)
minor injuries/ fractures
• CRPS type II (causalgia) develops after injury to
a major peripheral nerve.

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7. Pathohysiology
Exacly Mechanisme is still poorly understood
Both peripheral & central factors
• Altered cutaneous innervation following injury
• Peripheral sensitization- ↑substance P, bradykinin
• Central sensitization-↑ substance P, bradykinin, glutamate in
the spinal cord
- wind- up
• Sympathetically mediated pain- sympathoafferent coupling
• Inflammatory mediators-IL-2, IL-6, substance P, CGRP
• Cortical reorganization- altered processing
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multifactorial process involving both peripheral and central mechanisms

9. Complex Regional Pain Syndrom
“STAM”
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10. Stages
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No definitive sequence of stages occurs in all patients.

11. CRPS Stage 1 (Acute)
Immediately after injury (within weeks of injury)
MOST LIKELY TO BE REVERSED AND CURED
 SKIN: Red, warm, swollen, dry, inflamed.
 DISTRIBUTION: Pain is not compatible with a single peripheral
nerve, trunk, or root lesion.
 SYMPATHETIC:
-VASOMOTOR: Disturbances occur with variable intensity, producing
altered color and temperature
– SUDOMOTOR: Hyperhydrosis
• MOTOR: Decreased ROM, weakness
• X-RAYS: Normal
• BONE SCAN: Increased uptake

12. Stage 1 (Acute)

13. CRPS Stage 2 (Dystrophic)
within months of injury
• SKIN: Cool, moist, tight/shiny, swelling,
coarse/sparse hair, brittle nails, discolored,
edema
• SYMPATHETIC:
– VASOMOTOR: Mottled/cyanotic
– SUDOMOTOR: Hyperhydrosis
• MOTOR: Weakness, decreased ROM
• BONE SCAN: No longer helpful.

14. Stage 2 (Dystrophic)

15. CRPS Stage 3 (Atrophic)
• Pain is somewhat decreased
– less at rest, worse with passive motion
• Changes are irreversible
• SKIN: Atrophy, “waxy”, very thin, ulcerations, brittle
nails
• SYMPATHETIC:
– VASOMOTOR: Cold, intermittently cyanotic/mottled
• MOTOR: Decreased ROM, weakness, muscle &
tendon atrophy, contractures, dystonia, tremor.
Nonfunctional limb.
• X-RAYS: Diffuse patchy osteoporosis (Sudeck’s
Atrophy)

16. Atrophic Stage 3
Contractures
Skin Ulceration

17. Daignostic Criteria
• Because the pathophysiological
mechanisms of CRPS are not fully
understood, mechanism based diagnosis
is not yet feasible
– The diagnosis of CRPS is based solely on
clinical signs and symptoms (BUDAPEST
CRITERIA 2012).
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18. Budapest Criteria 2012
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19. Investigations
• objective testing (thermography, triple
phase bone scan, quantitative sudomotor
axon reflex test) is not necessary to make
the diagnosis, but in some cases may be
used to support a clinical diagnosis
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20. Investigations
• There is no specific diagnostic test available
for CRPS
• Main purpose: to exclude other diagnoses
– Lab: CBC,ESR,CRP to exclude
infection/rheumatologic
– Duplex / Ultrasound: exclude peripheral vasc
disease
– NCV studies: exclude peripheral neuropathic
disease, painful
• Imaging: may demonstrate osteoporosis in
affected limb (but no diagnostic value)
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21. Investigation Diagnostic block are
usefull?
• Sympathetic Blockade
(pain relief, increase
temperaturesuccesfull
block)
– Stellate Ganglion
Block
– Lumbar Sympathetic
Block
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22. Differential Diagnosis
1. Neuropathic pain
syndrome
2. Vascular diseases
3. Cellulitis
4. Inflammation
5. Myofascial pain
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23. Treatment
• Two types of treatment
1. Conservative treatment
• Most important: early active mobilization physical
therapy combined with pharmacotherapy,
psychological therapy
2. Interventional management
• Sympathetic block
• Spinal cord stimulator
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24. Conservative Treatment
• Multidisciplinary approach
• Pharmacotherapy
– Steroids- acute phase- oral prednisolone 30- 40
mg/day
– Anticonvulsants
– Antidepressants
– Lidocaine patch
– Opioids
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25. antidepressants
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26. Anti convulsants
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27. Oioids
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28. others
• Calcitonin
• Biphosphonates
• Vit.c
• N-acetylcysteine

29. Interventions
• Sympathetic block (stellate/lumbar block)
–Break the vicious cycle of pain.
–Permit more vigorous physical activity.
• Neurolytic blocks
–give excellent results when performed early.
–Diagnostic blocks using LA should be done
prior to neurolytic block
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30. Interventions
• Spinal cord stimulation
alters neuro chemistry in dorsal horns,
suppresing the hyperexcitability, increase
GABA
• Peripheral nerve stimulation
• Intrathecal drug delivery system-Used
for patients with dystonia , failed
neurostimulation, long standing disease, multi
limb involvement or need palliative care.
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31. Remember
• Treatment should be immediate after diagnosis.
• Multidisciplinary approach
• Aim treatment:
– toward restoration of full function of the affected
area.
• Intensity of therapy (in particular physiotherapy)
should be adapted to the severity of the disease.
– Gentle and below pain threshold and must not
exacerbate the pain since every painful stimulus may
worsen the syndrome
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